Hippocampal involvement in MDD is confined to principal substructures only. 3 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hippocampal involvement in MDD is confined to principal substructures only. 3 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction plays a central role in Alzheimer's disease (AD), since it drives the cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early life experience influences stress reactivity and mental health through effects on cognitive-emotional functions that are, in part, linked to gene expression in the dorsal and ventral hippocampus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Trans-diagnostic, domain- or symptom-focused approaches have been heralded as advancing psychiatric research, but relatively few clinical research programmes have been undertaken to leverage their potential. 1 key finding →
Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source
Careful design and user-testing should be made a priority in the development of computerized assessment interfaces, as well as reevaluating the cognitive assessment process to minimize patient anxiety and discomfort. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With a rapidly aging global human population, finding a cure for late onset neurodegenerative diseases has become an urgent enterprise. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
As our brains age, we tend to experience cognitive decline and are at greater risk of neurodegenerative disease and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Excitatory neurons are preferentially impaired in early Alzheimer's disease but the pathways contributing to their relative vulnerability remain largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Further analysis of the AD brain proteome will continue to yield new insights into the biological basis of AD. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Ligands targeting tau for use with positron emission tomography have rapidly been developed during the past several years, enabling the in vivo study of tau pathology in patients with Alzheimer's disease and related non-Alzheimer's disease tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Alzheimer's Association's Research Roundtable met in November 2016 to explore how best to measure changes in cognition and function in the preclinical stage of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD) and other tauopathies, the cytosolic protein Tau misfolds and forms intracellular aggregates which accumulate within the brain leading to neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Globally, approximately one in three of all adults suffer from multiple chronic conditions (MCCs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The adult quiescent blood-brain barrier (BBB), a structure organised by endothelial cells through interactions with pericytes, astrocytes, neurons and microglia in the neurovascular unit, is highly regulated but fragile at the same time. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Strong evidence has emerged recently for the concept that herpes simplex virus type 1 (HSV1) is a major risk for Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is a progressive neurodegenerative disease where biomarkers for disease based on pathophysiology may be able to provide objective measures for disease diagnosis and staging. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The temporal analysis of spontaneous speech can be exploited in implementing a new, automatic detection-based tool for screening MCI for the community. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment (MCI) is the prodromal stage of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is characterized by a cascade of biomarkers becoming abnormal, the pathophysiology of which is very complex and largely unknown. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome, caused by trisomy of chromosome 21, is the single most common risk factor for early-onset Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Being treatable, steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), or Hashimoto's encephalopathy, should be distinguished from untreatable conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A pathogenic mutation in the PSEN2 gene in a Korean patient associated with EOAD was identified. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[18F]Flortaucipir is a PET tau tracer used to visualize tau binding in Alzheimer's disease (AD) in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →